When functioning properly, a heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout a circulatory system. This intrinsic rhythm is a function of electrical signals generated by the sinoatrial node, or SA node, located in the upper right atrium of the heart. The SA node periodically depolarizes, which in turn causes the atrial heart tissue to depolarize such that right and left atria contract as the depolarization travels through the atrial heart tissue. The atrial depolarization signal is also received by the atrioventricular node, or AV node, which, in turn, triggers a subsequent ventricular depolarization signal that travels through and depolarizes the ventricular heart tissue causing the right and left ventricles to contract.
Some patients, however, have irregular cardiac rhythms, referred to as cardiac arrhythmias. An arrhythmia, in general, is a disturbance in the normal rate, rhythm or conduction pattern of the heart. Cardiac arrhythmias may result in diminished blood circulation because of diminished cardiac output. Atrial fibrillation is the most common cardiac arrhythmia and it reduces the pumping efficiency of the heart. Atrial fibrillation is characterized by rapid, irregular, uncoordinated activation waves conducting in various directions over the atria that, as a result, do not produce a coordinated, effective contraction. Without atrial contraction, the ventricles are less optimally filled before their contraction, which may lead to a reduced cardiac output. This reduced pumping efficiency due to atrial fibrillation requires the ventricle to work harder, which is particularly undesirable in sick patients who cannot tolerate additional stress. Although atrial fibrillation episodes are generally not life-threatening, they may be associated with extreme symptoms, a reduced quality of life, a reduced cardiac output and unpleasantly rapid and irregular heart rates being felt by the patient. Due to the lack of atrial contraction during atrial fibrillation, clots may form in the stagnant blood in the atria which, if they dislodge from the left atrial endocardium, may occlude small arteries in the brain or other organs, causing stroke. This is why patients with atrial fibrillation must take anticoagulant therapy.
For heart patients having a multi-chamber pacemaker, atrial fibrillation episodes present an additional problem, in that the pacemaker may coordinate ventricular pacing with atrial activity. When an atrial fibrillation episode begins, it is undesirable for ventricular pacing to be timed according to this pathological atrial activity. Accordingly, some pacemakers are equipped with “mode switching” capability that automatically switches to a non-tracking mode, such as DDIR, when atrial fibrillation is detected.
In patients with an implantable cardioverter defibrillator, atrial fibrillation may cause such high ventricular rates that the device incorrectly delivers therapy for ventricular tachycardia or fibrillation which can be very unpleasant for the patient. Additionally, in patients with heart failure and an implanted cardiac resynchronization device, the occurrence of atrial fibrillation not only compromises cardiac output because the ventricles are no longer optimally filled by atrial contractions, but present resynchronization devices loose effectiveness when they cannot synchronize to a regular atrial activation.
When an atrial fibrillation episode occurs, the pacemaker or another medical device may apply therapy to attempt to terminate the irregular arrhythmia. Therapy may include applying a shock or delivering a drug. While maintaining a high heart rate has been demonstrated to reduce the incidence of atrial fibrillation episodes in some patients (overdrive pacing), only defibrillation shocks are effective to terminate an ongoing atrial fibrillation episode. Anti-tachy pacing therapies may terminate episodes of atrial flutter (a regular but overly fast atrial rhythm) but have not been demonstrated to terminate atrial fibrillation.